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Requirement for Ascorbic Acid in a Rat Mutant Unable to Synthesize Ascorbic Acid¹

Department of Agricultural Chemistry, Nagoya University, Nagoya 464 Japan ^* Aburahi Laboratories, Shionogi Research Laboratories, Shionogi & Co., Ltd., Gotanda, Koga-gun, Shiga 520-34, Japan

The activities of several enzymes involved in hepatic ascorbic acid synthesis and the requirement of dietary ascorbic acid were investigated in the OD (osteogenic disorder) rat, which has a hereditary defect in ascorbic acid-synthesizing ability. No activity of hepatic L-gulonolactone oxidase was detected in OD rats. However, OD rats maintained the normal activities of hepatic UDPglucose dehydrogenase, UDPglucuronyl transferase and ß-glucuronidase. Hemorrhage in muscle and leg joints, lower hepatic content of cytochrome P-450 and lower activities of hepatic drug-metabolizing enzymes, higher serum and adrenal levels of corticosterone and lower urinary excretion of hydroxyproline were observed in ascorbic acid-deficient OD rats than in OD rats fed 300 mg ascorbic acid/kilogram diet. Consequently, we conclude that OD rats cannot synthesize ascorbic acid because of the lack of activity of hepatic L-gulonolactone oxidase and that the dietary addition of about 300 mg ascorbic acid (per kilogram diet) is enough to prevent signs of vitamin C deficiency and to achieve maximum growth, and that more than 300 mg ascorbic acid per kilogram diet may be required for the maximum activity of hepatic drug-metabolizing enzymes.

KEY WORDS: • ascorbic acid • OD rat (osteogenic disorder rat)

¹ Supported in part by a grant from the Vitamin C Research Committee in Japan.

² To whom reprint requests should be addressed.

Manuscript received 4 March 1985. Revision accepted 9 August 1985.

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